炎症体
目标2
上睑下垂
生物
NLRC4型
先天免疫系统
吡喃结构域
细胞生物学
效应器
NLRP1
半胱氨酸蛋白酶1
程序性细胞死亡
半胱氨酸蛋白酶
免疫系统
炎症
免疫学
遗传学
细胞凋亡
作者
Katherine C. Barnett,Sirui Li,Kaixin Liang,Jenny P.‐Y. Ting
出处
期刊:Cell
[Elsevier]
日期:2023-05-01
卷期号:186 (11): 2288-2312
被引量:132
标识
DOI:10.1016/j.cell.2023.04.025
摘要
Inflammasomes are critical sentinels of the innate immune system that respond to threats to the host through recognition of distinct molecules, known as pathogen- or damage-associated molecular patterns (PAMPs/DAMPs), or disruptions of cellular homeostasis, referred to as homeostasis-altering molecular processes (HAMPs) or effector-triggered immunity (ETI). Several distinct proteins nucleate inflammasomes, including NLRP1, CARD8, NLRP3, NLRP6, NLRC4/NAIP, AIM2, pyrin, and caspases-4/-5/-11. This diverse array of sensors strengthens the inflammasome response through redundancy and plasticity. Here, we present an overview of these pathways, outlining the mechanisms of inflammasome formation, subcellular regulation, and pyroptosis, and discuss the wide-reaching effects of inflammasomes in human disease.
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